32 research outputs found

    Posttraumatic Stress in Women after the September 11 Terrorist Attacks in New York City

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    Background: Women have been shown to be at higher risk than men of developing posttraumatic stress disorder (PTSD) after traumatic events. Women in New York City were more likely than men to have probable PTSD 5–8 weeks after the September 11, 2001, terrorist attacks on the World Trade Center. We explored the factors that could explain the higher prevalence of probable PTSD among women in the aftermath of the attacks. Methods: Data from a telephone survey of a randomly selected group of residents of Manhattan living south of 110th street, conducted 5–8 weeks after September 11, were used in these analyses. The survey assessed demographic information, lifetime experience of traumatic events, life stressors, social support, event exposure variables, perievent panic attacks, postevent concerns, and probable PTSD related to the attacks. We determined the contribution of key covariates that could explain the gender-probable PTSD relation through stratified analyses and manual stepwise logistic regression model building. Results: Among 988 respondents, women were two times more likely than men to report symptoms consistent with probable PTSD after the September 11 attacks. When adjusted for potential confounders, the association between gender and probable PTSD diminished from OR 5 2.2 (95% confidence interval [CI] 1.3–3.6) to OR 5 1.2 (95% CI 0.7–2.2). Conclusions: These results suggest that specific behavioral and biographic factors (including previous traumatic experiences and psychological disorders, social responsibilities, and perievent emotional reactions) explained most of the excess burden of probable PTSD among women after a disaster. Isolating the characteristics that place women at greater risk for probable PTSD after disasters can inform public health prevention strategies and spur further research.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/40341/2/Pulcino_Posttraumatic Stress in WOmen after_2003.pd

    Interrelationships between serum levels of amiodarone, desethylamiodarone, reverse T3 and the QT interval during long-term amiodarone treatment

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    The interrelationships between serum levels of amiodarone, desethylamiodarone, and reverse T3, and changes in the corrected QT interval ([Delta]QTc) were examined in 22 patients during long-term treatment with amiodarone. At 1, 3, and 6 months of follow-up, the correlation coefficient between serum levels of amiodarone or desethylamiodarone and reverse T3 ranged from 0.01 to -0.2 (p > 0.4). At the same time intervals, the correlation coefficient between both amiodarone and desethylamiodarone levels and [Delta]QTc ranged from 0.1 to -0.1 (p > 0.6), and the correlation coefficient between reverse T3 and [Delta]QTc also ranged between 0.1 to -0.1 (p> 0.5). Substituting percent [Delta]QTc for [Delta]QTc also did not reveal a significant correlation. These data demonstrate that serum levels of reverse T3 cannot be used as a substitute for serum levels of amiodarone in monitoring patients being treated with amiodarone. The absence of a correlation between serum reverse T3 levels and [Delta]QTc suggests that the delay in repolarization which occurs during amiodarone therapy is not secondary to an amiodarone-induced abnormality in thyroid hormone metabolism.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26433/1/0000521.pd

    Lifestyle modification and metformin as long-term treatment options for obese adolescents: study protocol

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    <p>Abstract</p> <p>Background</p> <p>Childhood obesity is a serious health concern affecting over 155 million children in developed countries worldwide. Childhood obesity is associated with significantly increased risk for development of type 2 diabetes, cardiovascular disease and psychosocial functioning problems (i.e., depression and decreased quality of life). The two major strategies for management of obesity and associated metabolic abnormalities are lifestyle modification and pharmacologic therapy. This paper will provide the background rationale and methods of the REACH childhood obesity treatment program.</p> <p>Methods/design</p> <p>The REACH study is a 2-year multidisciplinary, family-based, childhood obesity treatment program. Seventy-two obese adolescents (aged 10-16 years) and their parents are being recruited to participate in this randomized placebo controlled trial. Participants are randomized to receive either metformin or placebo, and are then randomized to a moderate or a vigorous intensity supervised exercise program for the first 12-weeks. After the 12-week exercise program, participants engage in weekly exercise sessions with an exercise facilitator at a local community center. Participants engage in treatment sessions with a dietitian and social worker monthly for the first year, and then every three months for the second year. The primary outcome measure is change in body mass index and the secondary outcome measures are changes in body composition, risk factors for type 2 diabetes and cardiovascular disease, changes in diet, physical activity, and psychosocial well-being (e.g., quality of life). It is hypothesized that participants who take metformin and engage in vigorous intensity exercise will show the greatest improvements in body mass index. In addition, it is hypothesized that participants who adhere to the REACH program will show improvements in body composition, physical activity, diet, psychosocial functioning and risk factor profiles for type 2 diabetes and cardiovascular disease. These improvements are expected to be maintained over the 2-year program.</p> <p>Discussion</p> <p>The findings from this study will advance the knowledge regarding the long-term efficacy and sustainability of interventions for childhood obesity.</p> <p>Trial Registration</p> <p>ClinicalTrials.gov number NCT00934570</p

    Finishing the euchromatic sequence of the human genome

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    The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

    Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

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    The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)

    Effects of Healing Touch on Postsurgical Adult Outpatients

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    This prospective pilot study was implemented to determine whether a Healing Touch (HT) treatment postoperatively would have an effect on pain, anxiety, blood pressure, and pulse rate in adult postoperative outpatients. Using a randomized control trial design, participants were assigned to a control or intervention group. The control group received traditional nursing care (TNC), and the intervention group received a HT treatment in addition to TNC. Pre- and postdata collection included measurement of pain, anxiety, blood pressure, and pulse. HT treatment was at least as effective as TNC for reduction in pain and more effective in reducing anxiety. Posttreatment anxiety ratings in the intervention group had a significant decrease (0.55; p = .029), while the reduction in anxiety in the control group was not significant (0.25; p = .22). Neither group showed any difference pre- versus posttreatment in blood pressure or pulse. The intervention group had a decrease in pain rating of 1.0 (p \u3c .001), and the control group had a decrease of 0.64 (p = .02). There was a trend toward a decrease in the use of narcotics with HT. HT is an appropriate modality to decrease anxiety, may be appropriate for pain reduction, and may decrease the amount of narcotics needed postoperatively. Patient comments reflected the relaxing effects of receiving HT. The findings support the use of HT as an effective complementary intervention for surgical outpatients, however additional research is recommended

    Collaboration Among Community Members, Local Health Service Providers, and Researchers in an Urban Research Center in Harlem, New York

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    A majority of the world’s population will live in urban areas by 2007 and cities are exerting growing influence on the health of both urban and non-urban residents. Although there long has been substantial interest in the associations between city living and health, relatively little work has tried to understand how and why cities affect population health. This reflects both the number and complexity of determinants and of the absence of a unified framework that integrates the multiple factors that influence the health of urban populations. This paper presents a conceptual framework for studying how urban living affects population health. The framework rests on the assumption that urban populations are defined by size, density, diversity, and complexity, and that health in urban populations is a function of living conditions that are in turn shaped by municipal determinants and global and national trends. The framework builds on previous urban health research and incorporates multiple determinants at different levels. It is intended to serve as a model to guide public health research and intervention.http://deepblue.lib.umich.edu/bitstream/2027.42/40360/2/Galea_Collaboration Among Community Members, Local Health_2001.pd
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